essential role of mast cells in the visceral hyperalgesia induced by t. spiralis infection and stress in rats肥大细胞的重要作用引起的内脏痛觉过敏t spiralis感染和压力的老鼠.pdfVIP

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essential role of mast cells in the visceral hyperalgesia induced by t. spiralis infection and stress in rats肥大细胞的重要作用引起的内脏痛觉过敏t spiralis感染和压力的老鼠.pdf

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essential role of mast cells in the visceral hyperalgesia induced by t. spiralis infection and stress in rats肥大细胞的重要作用引起的内脏痛觉过敏t spiralis感染和压力的老鼠

Hindawi Publishing Corporation Mediators of Inﬂammation Volume 2012, Article ID 294070, 8 pages doi:10.1155/2012/294070 Research Article Essential Role of Mast Cells in the Visceral Hyperalgesia Induced by T. spiralis Infection and Stress in Rats Chang-Qing Yang, Yan-Yu Wei, Chan-Juan Zhong, and Li-Ping Duan Department of Gastroenterology, Peking University Third Hospital, 49 North Garden Road, Haidian District, Beijing 100191, China Correspondence should be addressed to Li-Ping Duan, duanlp@ Received 16 September 2011; Accepted 18 December 2011 Academic Editor: Amal O. Amer Copyright © 2012 Chang-Qing Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Mast cells (MCs) deﬁcient rats (Ws/Ws) were used to investigate the roles of MCs in visceral hyperalgesia. Ws/Ws and wild control (+/ +) rats were exposed to T. spiralis or submitted to acute cold restraint stress (ACRS). Levels of proteinase-activated receptor 2 (PAR2) and nerve growth factor (NGF) were determined by immunoblots and RT-PCR analysis, and the putative signal pathways including phosphorylated extracellular-regulated kinase (pERK1/2) and transient receptor potential vanilloid receptor 1 (TRPV1) were further identiﬁed. Visceral hyperalgesia triggered by ACRS was observed only in +/ + rats. The increased expression of PAR2 and NGF was observed only in +/ + rats induced by T. spiralis and ACRS. The activation of pERK1/2 induced by ACRS occurred only in +/ + rats. However, a signiﬁcant increase of TRPV1 induced by T. spiralis and ACRS was observed only in +/ + rats. The activation of PAR2 and NGF via both TRPV1 and pERK1/2 signal pathway is